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Original Article
53 (
1
); 1-5

Incidence of Acute Mountain Sickness in patients of High Altitude Pulmonary Edema: Is the Lake Louise Scoring accurate?

Cl Spl (Physiology), Armed Forces Medical College, Pune-411 040

Abstract

Acute Mountain Sickness (AMS) affects 30-50% of healthy individuals rapidly ascending to altitudes greater than 9000 ft. AMS and High Altitude Cerebral Edema (HACE) are often considered two ends of the same disease spectrum. The relationship between AMS and High Altitude Pulmonary Edema (HAPE) is however, less known. The present study attempted to examine the co-existence of the two conditions. 254 cases of HAPE that occurred at 10500 ft in the Western Himalayas were studied to ascertain the co-existence of AMS using the Lake Louise Scoring System (LLS). Symptoms of HAPE developed in 2.8±2.2 days after arrival at altitude. The mean LLS in HAPE patients was 3.5±2.5. 41% of HAPE patients satisfied the clinical criteria of Acute Mountain Sickness based on the LLS. Those patients with early onset of symptoms of HAPE did not necessarily show higher LLS scores. AMS appears to co-exist in a large percentage of patients with HAPE if diagnosed using the LLS. Since the two clinical conditions do not share a common pathophysiology as per present understanding, it is possible that the LLS may return higher scores if used as a basis for diagnosing AMS once clinical features of HAPE have set in.

Keywords

Acute Mountain Sickness
High Altitude Pulmonary Edema
Lake Louise Scoring System

Introduction

Altitude medicine is rapidly gaining popularity as the number of visitors to High Altitude (HA) has been increasing steadily over the years. The responses of the human body to the environmental challenges of high altitude have been studied for many years now and interesting insights gained into the pathophysiology of high altitude illnesses. These illnesses largely comprise of Acute Mountain Sickness (AMS), High Altitude Cerebral Edema (HACE) and High Altitude Pulmonary Edema (HAPE).

AMS is a largely benign and self limiting condition, provided it is recognized in time and further ascent prevented till symptoms subside. The incidence varies depending on the altitude and rate of ascent and has been reported varying from 3.1% at 6,600 ft [1] to values of 53% at 15,044 ft [2]. HAPE occurs with an incidence that again varies with the altitude and rate of ascent, but in addition also depends on physical exertion at altitude, gender and individual susceptibility. Indian soldiers rapidly air lifted to 11,500 ft from sea level developed HAPE with an incidence that varied from 2.3% to 15% [3] while Menon reported an incidence of 0.57% in a similar group of soldiers [4].

In terms of their pathophysiology, AMS and HAPE are thought to represent the effects of hypoxia on two different physiological systems, the central nervous system and the pulmonary system respectively. Interestingly, the association between the two conditions has remained controversial. Reports by Singh [3] and Larson [5] suggested that a fairly large percentage of HAPE patients have AMS as a preceding illness. However, more recent reports suggest no association between the two conditions [6,7]. The present study examined the clinico-epidemiological data of 254 cases of HAPE occurring at an altitude of 11,000 ft above mean sea level to determine the incidence of AMS in patients of HAPE at the time of their reporting to a medical facility.

Material and Methods

Clinical data of 254 cases of HAPE was tabulated and organized for the analysis. AMS was diagnosed using the Lake Louise Score [8] with a self reported score of = 4 being taken as the diagnostic criteria as shown in Appendix A.

The diagnosis of HAPE was based on the Lake Louise criteria as well and involved the following:

  1. Recent ascent to 11,000 ft.

  2. Symptoms consisting of breathlessness, cough, chest discomfort, fatigue (at least two).

  3. Clinical signs of crackles/rhonchi on chest auscultation, tachycardia, tachypnea or central cyanosis (any two).

  4. No history or clinical findings suggestive of respiratory infection, pulmonary thromboembolism or underlying cardio-pulmonary disease.

  5. Features of pulmonary edema on chest X-ray where available.

Results

The mean age of the patients was 30.1 ± 8.8 years. All the 254 cases were males. None of the patients gave a history of HAPE in the past.

Mode of travel to high altitude. 203 of the 254 cases (79.9%) had traveled to high altitude by air, taking about 80 minutes to reach an altitude of 11,000 ft from sea level while 51 of the cases (20.1%) had arrived by road to same altitude taking between 2 to 4 days to travel from sea level to an altitude of 11,000 ft.

Time of onset of symptoms. The time frame of development of symptoms of HAPE in the cases studied is also shown in Table 1. The majority of patients developed symptoms within the first 4 days of arrival at altitude (87.23%). The average time of onset of symptoms was 2.8 ± 2.2 days after arrival at high altitude.

Table 1:: Time of onset of symptoms in cases with HAPE
Day of arrival at HA Number who developed symptoms
Day 1 75(31.9%)
Day 2 56(23.8%)
Day 3 46(19.6%)
Day 4 28(11.9%)
Day 5 8(3.4%)
Day 6 5(2.1%)
Day 7 8(3.4%)
Beyond Day 7 9(3.8%)

Evidence of AMS and or HACE. The mean self reported Lake Louise Score recorded on admission to a medical facility was 3.5 ± 2.5. 41% of the patients reported a score of equal to or more than 4. Only one of the patients (0.4%) was found to be drowsy and disoriented and demonstrated gait ataxia. He was diagnosed and managed as a case of HAPE with HACE. There was no correlation between the day of occurrence of HAPE and Lake Louise Score for AMS.

Discussion

As has been reported earlier, rapid induction to high altitude poses a greater risk of developing high altitude illness, the sleeping altitude, previous history of high altitude illness and individual susceptibility being other predisposing factors. The same is evident from the above data which shows that almost 80% of the cases of HAPE had traveled to 10,500 ft from sea level by air, a journey lasting about 80 minutes on an average. The symptoms of HAPE are known to develop within the first four days at altitude [6] and in the present series more than 87% of the cases occurred during the first 4 days at 10,500 ft with a mean time of onset of 2.8± 2.2 days. Comparable time frames for development of symptoms of HAPE have been reported in literature [9,10,11]. The symptoms reported by the patients in this study merit attention. While symptoms of breathlessness, chest discomfort and cough are the commonest symptoms associated with HAPE, a large percentage of patients in this study group were found to complain of headache, dizziness and vomiting. These three symptoms were not necessarily restricted to those patients who developed symptoms comparatively early on reaching high altitude.

The association of AMS and HAPE has been explored but conclusive evidence remains elusive. Occurrence of headache and nausea in 53% and 35% patients respectively has also been reported by Hultgren in a series of 150 cases [10]. In a series of 27 HAPE patients in Japan, 62.9% were found to have symptoms of headache, nausea and vomiting [12]. 53% of HAPE patients at moderate altitude were also found to complain of headache [13]. None of the above case series, however, mention how many of their patients could also be labeled as suffering from AMS.

While on one hand, it has been reported that abnormalities on Chest X-rays are not very common in patients with AMS [14,15] and HAPE is not necessarily preceded by AMS [6,7], reports of AMS being present in upto 80% of HAPE patients have also been published [3,5]. In an interesting study, 15% of climbers to an altitude of 15,088 ft were found to have evidence of sub-clinical pulmonary edema and higher Lake Louise scores than those who did not show evidence of pulmonary edema [16]. 30% of trekkers with AMS in Nepal were also seen to have rales [17]. However, unlike the present study, none of these individuals developed clinically significant illness to warrant treatment. In the present series of 254 cases, 41% of HAPE patients satisfied the Lake Louise criteria for diagnosis of AMS with a self reported score of = 4. Our data suggests the two conditions can coexist in a fairly large percentage of patients, though not in 80% of patients as reported. Also, unlike earlier reports of AMS occurring as a prodrome in HAPE patients [3,5], our data suggests the same may not always be true. It is possible that the self reported LLS may be high in patients already suffering from HAPE since symptoms of reduced appetite, sleep disturbances and fatigue, which figure on the LLS questionnaire, may be part of the general symptom complex of feeling unwell as is likely in all ill patient, HAPE not being an exception. This fact may lead to high self reported LLS in such patients.

Conclusion

The present series of 254 cases of HAPE in the Western Himalayas is probably the largest series reported. The association between AMS and HAPE remains unclear. A fairly large percentage of HAPE patients would qualify as suffering from AMS if the Lake Louise Scoring system is used to diagnose AMS. The fact that patients who develop HAPE on the very first or second day at HA do not necessarily have higher Lake Louise Scores for AMS may suggest no co-relation between the two conditions. However, since no gold standard exists for diagnosing AMS, it is difficult to comment on the accuracy of this scoring system to diagnose AMS if co-morbid conditions exist in the patient.

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